Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with multiple organ damage. Several studies have found that, in addition to significant production of autoantibodies, the majority of SLE patients exhibit increased expression of type I interferon (IFN-I) regulated genes (also known as IFN-I traits), and that IFN-I plays a crucial role in the pathogenesis of SLE. In SLE, virtually all immune cells are dysregulated, and most of these aberrant dysregulations are directly or indirectly affected by IFN-I. The mechanism of action of IFN-I in these immune cells is multifaceted. In this review, we focus on the immune cell types that produce IFN-I and are affected by IFN-I in SLE. Importantly, we explore the research progress of related drugs in terms of IFN-I production, itself, and downstream. Here we provide the most up-to-date information on the mechanisms that lead to the pathogenesis of SLE, providing the basis for the development of innovative future therapies and future research directions.